We demonstrate that continuous phase fat structuring affects the release of a model marker from the dispersed aqueous phase of water-in-oil (W/O) emulsions subjected to simulated gastrointestinal conditions. Model W/O emulsions consisting of a 20 wt% dispersed aqueous phase containing 1 mM methylene blue added as a marker were stabilized via either continuous phase core-shell stabilization, network stabilization or a combination thereof. The network-stabilized emulsion showed the lowest extent of marker release under gastric (<3% after 1 h) and duodenal conditions (~5% after 2 h). The independent contributions of dilution, osmotic gradient, pH and bile salts all affected emulsion stability and marker release, with bile salts showing the greatest contribution. The key finding of this study was that the presence of a fat crystal network provided greater resistance against marker release than core-shell emulsion stabilization during in vitro digestion. Overall, this study has shown that fat phase structuring is a key parameter to control W/O emulsion breakdown and marker release. • Emulsion in-vitro digestion behavior is dependent on stabilization mechanism. • Time, dilution and digestion fluid composition affect emulsion breakdown and marker release. • Gastric environment ionic strength and temperature contribute to droplet growth. • Duodenal conditions promote extensive degradation of core-shell emulsions. • Presence of a solid fat network restricts droplet migration and bile salt action.